Systemic lupus erythematosus is an autoimmune disorder affecting multiple organ systems. Patients with systemic lupus erythematosus exhibit a bimodal pattern of mortality, with those who have had the disease for 5 to 10 years being at increased risk of cardiovascular disease, particularly myocardial infarction. Elevated levels of conventional cardiovascular risk factors promote vascular damage resulting in impairment of normal endothelial function. In addition, autoantibodies directed against oxidised lipoproteins, along with chronic secretion of inflammatory cytokines and suppression of fibrinolytic parameters, are thought to increase atherogenesis. Treatment with corticosteroids may also contribute to the accelerated atherosclerosis observed in these patients. This review discusses the accentuated relationship between conventional cardiovascular risk factors, systemic lupus erythematosus–induced inflammatory changes and the early stages of atherogenesis and how careful monitoring of risk factors and use of appropriate therapies may reduce the progression of atheroma development in patients with systemic lupus erythematosus.

Scientific evidence is emerging to indicate that motor neuron injury in motor neuron disease may reflect a complex interplay between genetic factors, oxidative stress, and imbalance of the glutamatergic excitatory control of motor neurons, which may result in damage to critical target proteins and organelles. The relative importance of these factors is likely to vary in different subgroups of patients. Protein aggregation may play a role in some forms of motor neuron injury, and the eventual demise of motor neurons may occur by a programmed cell death pathway. Advances in symptomatic therapy for patients with motor neuron disease include the development of specialist clinics, with input from multidisciplinary teams, as well as hospice care in the late stages of the disease. A number of recent therapeutic trials of potential neuroprotective drugs have been conducted, including antiglutamate, antioxidant, and neurotrophic agents. To date, only the antiglutamate agent riluzole has been shown to reproducibly prolong the survival of patients with motor neuron disease. Future therapy in motor neuron disease is likely to include a ÔcocktailÕ of neuroprotective compounds to interfere with several molecular pathway that lead to neuronal injury. In using therapeutic strategies aimed towards retarding or arresting motor neuron disease, close attention will need to be paid to quality of life issues.